ArticleThe Journal of biological chemistry2012
XBP1S associates with RUNX2 and regulates chondrocyte hypertrophy.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- High doses of dexamethasone induce endoplasmic reticulum stress-mediated apoptosis by promoting calcium ion influx-dependent CHOP expression in osteoblasts.Molecular biology reports · 2021Article
- XBP1 signalling is essential for alleviating mutant protein aggregation in ER-stress related skeletal disease.PLoS genetics · 2019Article
- Cellular ageing mechanisms in osteoarthritis.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Review
- Inflammation and intracellular metabolism: new targets in OA.Osteoarthritis and cartilage · 2015Review
- Mineral trioxide aggregate induces osteoblastogenesis via Atf6.Bone reports · 2015Article
- Emerging regulators of the inflammatory process in osteoarthritis.Nature reviews. Rheumatology · 2015Review
- Explore on the effect of ATF6 on cell growth and apoptosis in cartilage development.Histochemistry and cell biology · 2014Article
- 17β-Estradiol inhibits ER stress-induced apoptosis through promotion of TFII-I-dependent Grp78 induction in osteoblasts.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- XBP1S, a BMP2-inducible transcription factor, accelerates endochondral bone growth by activating GEP growth factor.Journal of cellular and molecular medicine · 2014Article
- IRE1a constitutes a negative feedback loop with BMP2 and acts as a novel mediator in modulating osteogenic differentiation.Cell death & disease · 2014Article
- The Xbp1s/GalE axis links ER stress to postprandial hepatic metabolism.The Journal of clinical investigation · 2013Article
Corrections and comments
- Retraction · 2015-04-24Notice - Limited or No Information · · 1. Article withdrawn by authors
- Retracted
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BMP2 (bone morphogenetic protein 2) is known to activate unfolded protein response signaling molecules, including XBP1S and ATF6. However, the influence on XBP1S and ATF6 in BMP2-induced chondrocyte differentiation has not yet been elucidated. In this study, we demonstrate that BMP2 mediates mild endoplasmic reticulum stress-activated ATF6 and directly regulates XBP1S splicing in the course of chondrogenesis. XBP1S is differentially expressed during BMP2-stimulated chondrocyte differentiation and exhibits prominent expression in growth plate chondrocytes. This expression is probably due to the activation of the XBP1 gene by ATF6 and splicing by IRE1a. ATF6 directly binds to the 5'-flanking regulatory region of the XBP1 gene at its consensus binding elements. Overexpression of XBP1S accelerates chondrocyte hypertrophy, as revealed by enhanced expression of type II collagen, type X collagen, and RUNX2; however, knockdown of XBP1S via the RNAi approach abolishes hypertrophic chondrocyte differentiation. In addition, XBP1S associates with RUNX2 and enhances RUNX2-induced chondrocyte hypertrophy. Altered expression of XBP1S in chondrocyte hypertrophy was accompanied by altered levels of IHH (Indian hedgehog) and PTHrP (parathyroid hormone-related peptide). Collectively, XBP1S may be a novel regulator of hypertrophic chondrocyte differentiation by 1) acting as a cofactor of RUNX2 and 2) affecting IHH/PTHrP signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.